Atrial Fibrillation and Obstructive Sleep Apnea
Beyond the Pulmonary Veins
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See Article by Anter et al
Obstructive sleep apnea (OSA) is associated with an increase in morbidity and mortality and has been linked to the development and progression of atrial fibrillation (AF).1 Although AF shares important risk factors and comorbidities with OSA, such as obesity, hypertension, and diastolic dysfunction, recent advances in the understanding of direct effects of OSA on cardiac structure and function suggest a more causal link between OSA and AF independent of other comorbidities.2,3 Human and animal studies have reported adverse structural and electric changes in the atria, including left atrial (LA) stretch, voltage reduction, conduction slowing, diffuse distribution of complex atrial electrograms, and altered atrial tissue refractoriness in patients with OSA out of proportion to age, AF chronicity, and other risk factors. The common denominator is atrial fibrosis, which promotes arrhythmogenesis. Dysautonomia has also been suggested to play a role in apnea-induced AF.
OSA is predictive of AF recurrences after catheter ablation (CA) of AF.4,5 The poor ablation outcome in this group of patients seems to be independent of comorbid obesity and LA size. However, the precise mechanisms underlying the association between OSA and higher probability of recurrent AF after CA have not been well understood.
The prospective, observational study by Anter et al6 in this issue of Circulation: Arrhythmia and Electrophysiology provides important mechanistic insights. This rigorously designed investigation sought to characterize the atrial substrate, and the frequency and significance of non–pulmonary vein (PV) triggers in patients with paroxysmal AF and OSA referred for CA. The study group consisted of 43 patients with paroxysmal AF and recently diagnosed, previously untreated, moderate-to-severe OSA who underwent PV isolation (PVI) and …